We use cookies to understand how you use our site and to improve your experience. This includes personalizing content and advertising. To learn more, click here. By continuing to use our site, you accept our use of cookies. Cookie Policy.

The self-expanding, tubular endoprosthesis is composed of polyester fabric and a nitinol stent scaffold in a tubular configuration; non-resorbable sutures attach the stents to the fabric. In addition, platinum-iridium radiopaque markers are sewn to the fabric to allow radiographic visualization of the edges of the graft material, and to provide a guide to the minimum overlap distance required when multiple stent grafts are used. Three proximal spherical markers and the two distal spherical markers indicate the extremities of the covered stent graft, with mid graft markers indicating a potential overlap edge.

The Valiant Navion stent graft is pre-loaded and delivered through the femoral or iliac artery to the site of the lesion using the Valiant Navion delivery system over a guidewire. Upon deployment, the stent graft self-expands due to the superelastic properties of the nitinol stents. The proximal and distal ends of the stent graft are designed to conform to the shape and size of the proximal and distal seal zones due to the radial force of the stents. The Valiant Navion Delivery System is available in an outer diameter of 18, 20, and 22 Fr and a working length of 93 cm.

“Our focus at Medtronic continues to be on advancing the treatment of complex aortic disease to improve outcomes and extend life,” said John Farquhar, vice president and general manager of the Aortic business at Medtronic. “FDA approval now makes it possible for more patients with thoracic aortic disease to receive endovascular repair. This therapy is truly a testament to our more than 20 years of clinical and engineering insights, and we look forward to making it available to those in need.”

TAA results from continuous dilation of the descending thoracic aorta as a result of the degradation of structural proteins such as collagen and elastin, which eventually leads to medial degeneration and weakening of the aortic wall. Subsequent dilatation results from hemodynamic forces and intrinsic changes in the composition of the arterial wall, which cause the aorta to expand further and increase wall tension, creating a vicious cycle and eventual life-threatening rupture and hemorrhage.